Hypertension, Hyperlipidemia: Are our children safe? Patrick R

Hypertension, Hyperlipidemia:
Are our children safe?
Patrick R
Hints and exam tips
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HTN is a hot topic for exams – particularly, what
is really malignant HTN and who needs urgent
treatment.
Also be sure that you know how to recognize the
secondary causes of HTN
Lipids are less beloved by examiners though
they do like to ask about niacin and flushing
Cardiovascular risk in your clinic
patients
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Do not approach HTN, Hyperlipidemia as
individual problems.
Look upon them as part of your patients
cardiovascular risk profile – once your patients
understand that they are changing their lifestyle
and taking meds to lower their risks of stroke,
heart attack, kidney disease and peripheral
vascular disease they will be more likely to
follow your advice
Consider does your pt have the “metabolic
syndrome”
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Any 3 of
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obesity, high TG, low HDL, HTN, impaired glucose tolerance
Who are my at risk patients – who
should I be screening?
(basically everyone!)
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Obesity
Dyslipidemia – all pts need fasting lipid profile
DM
Smoking
Lack of exercise
Age >55 for men, >65 for women
FHx of premature cardiovascular disease
Microalbuminuria in diabetics
Hypertension
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Management should be based on the “JNC-7” guidelines
Treatment should be instituted at >140/90 in most pts or
>130/80 in pts with DM or chronic kidney disease
Stage II HTN is >160/100 and only important to
distinguish because these patients usually need 2 drugs
to control.
Making 1st diagnosis needs 2 readings at least 5 mins
apart and in both arms. Many doctors will actually get
two readings a week or two apart in a previously
undiagnosed patient, and many patients will be resistant
to start therapy without more than one reading
Ambulatory BP monitoring can be used to evaluate for
white coat HTN, and also helpful in assessing response
to therapy, or persuading a pt that he needs treatment
New diagnosis of HTN
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Assess other cardiovascular risk factors
Look for reversible causes of HTN
Look for evidence of end organ damage
Renal
 Retinal
 Cardiac – check EKG, consider stress test if any
history of angina type symptoms
 CNS – take full Hx and evaluate for previous TIA.
Check for carotid bruits
 Peripheral artery disease – check for AAA and distal
pulses
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Lifestyle modification
Medication
A 56-year-old man undergoes a routine physical examination. A
funduscopic examination is performed.
What does the funduscopic photograph show?
( A ) Arteriolar sclerosis and hypertensive retinopathy
( B ) Diabetic proliferative retinopathy
( C ) Papilledema
( D ) Malignant hypertensive retinopathy
Correct Answer = A
Characteristic changes are noted in the retinas of patients with longstanding
hypertension. Narrowing of the terminal branches of retinal arterioles may
be seen, as well as general narrowing of vessels with severe local
constriction (as shown in this photograph).
As the disease progresses, striate hemorrhages and soft exudates become
visible. In a normal eye, retinal arterioles are transparent, so that blood flow
is visible during ophthalmoscopy. A light streak from the ophthalmoscope
will reflect from the convex wall of the healthy arteriole. In a sclerotic
arteriole, thickening and fibrosis of the vessel wall develop as the sclerosis
progresses. The central light reflex increases in width, and the walls of the
vessel look like burnished copper, producing a "copper-wire" arteriole.
With further progression and additional fibrosis, the entire width of the
arteriole reflects the white stripe, producing "silver-wire" arteries. This
patient's funduscopic photograph shows both the "copper and silver wires"
characteristic of arteriolar sclerosis and the characteristic changes of
hypertensive retinopathy.
A 62-year-old hypertensive woman is evaluated because of headaches and
confusion. After her vital signs are recorded, a funduscopic examination is
performed.
Based on the funduscopic examination, which of the following
conditions most likely present?
( A ) Optic neuritis
( B ) Arteriolar sclerosis
( C ) Brain tumor
( D ) Malignant hypertension
Correct Answer = D
The retinal changes associated with malignant hypertension
consist of arteriolar narrowing, severe local vasoconstriction,
hemorrhages, exudates, and papilledema. The exudates are
caused by fibroid necrosis of vessel walls. Papilledema
associated with malignant hypertension can be differentiated
from papilledema due to other causes by its clinical context.
Optic neuritis, generally monocular and another cause of a disk
swelling, is not associated with hypertension and will have
accompanying afferent pupillary defects and loss of vision. Both
papilledema associated with malignant hypertension and optic
neuritis can be accompanied by loss of vision. Arteriolar
sclerosis is not accompanied by papilledema. Brain tumors can
be associated with papilledema but not arteriolar narrowing,
vasoconstriction, hemorrhages, or exudates.
Non-essential HTN
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Although most cases of HTN are essential HTN,
always consider whether it could be due to
another process.
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Sleep Apnea
Drug induced (esp cocaine, also drugs like NSAIDS, OCP)
Chronic renal disease
Renal artery stenosis
Cushing’s syndrome or treatment with steroids
Hyperaldosteronism
Pheochromocytoma
Coarctation of aorta
Thyroid and parathyroid disease
A 25-year-old man is evaluated because of several months of
episodic sweating, headaches, and palpitations. His medical
history includes surgical repair of ankle injuries sustained in a
fall while rollerblading 6 months ago; the anesthesiologist
noted that the patient's blood pressure fluctuated significantly
during the procedure and advised him to be evaluated for
possible hypertension.
On physical examination, he is 180 cm (71 in) tall and weighs
72 kg (158 lb); his pulse rate is 80/min, and his blood pressure
is 135/80 mm Hg. He has no goiter, lid lag, or tremor. Plasma
glucose was normal during an episode of palpitations. His
thyroid function tests are normal.
Measurement of which of the following is the best next
step in the evaluation of this patient?
( A ) Serum insulin and insulin-like growth factor 1
( B ) Repeat measurements of blood pressure
( C ) Catecholamines in a 24-hour urine sample
( D ) Thyroid stimulating hormone (TSH)
Correct Answer C
This patient has three classic symptoms that suggest pheochromocytoma:
headache, sweating, and palpitations, all of an episodic nature. The
diagnosis is further suggested by the history of labile blood pressure during
a recent surgical procedure.
The fact that he is not currently hypertensive does not argue against the
diagnosis, because many patients with pheochromocytoma have
hypertension only during their episodic paroxysms. Once suspected clinically,
the diagnosis is established biochemically with the finding of elevated
urinary secretion of catecholamines or their metabolites. Diagnostic yield is
highest when the collection is initiated with the onset of an episode. Though
rare, pheochromocytoma can be life threatening, and if it is considered in
the differential diagnosis of a patient’s symptoms, testing should be ordered.
Although some of the patient’s symptoms are suggestive of acromegaly or
stress, there are no other symptoms, historical features, or physical findings
that support these diagnoses. Physical examination does not suggest
hypothyroidism, and the normal results of thyroid function tests exclude this
diagnosis. A normal plasma glucose concentration during a symptomatic
episode excludes insulinoma.
A 41-year-old man is evaluated because of easy bruising. His medical history
includes recent onset of borderline diabetes mellitus, which is being treated
by diet. Review of systems shows a 4.6-kg (10-lb) weight gain, fatigue,
muscle weakness, decreased libido, and depression. He uses no drugs, quit
smoking 1 year ago, and has been drinking one to two six-packs of beer
nightly.
On physical examination, he is 183 cm (72 in) tall and weighs 91 kg (200
lb); his pulse rate is 88/min, and his blood pressure is 150/95 mm Hg. He
has a round face and supraclavicular and posterior cervical fullness. He has
plethoric facies, tinea versicolor of the chest, no petechiae, and three or four
ecchymoses on the extremities. Neurologic examination is normal, except
for 3/5 strength in proximal leg muscles.
Which of the following is the most likely diagnosis?
( A ) von Willebrand’s disease
( B ) Platelet dysfunction
( C ) Hemochromatosis
( D ) Cushing’s syndrome
( E ) Small vessel vasculitis
Correct Answer
D
This patient presents with clinical features suggestive of Cushing’s
syndrome. Urine-free cortisol is the best test to diagnose this disorder.
However, because of his recent heavy alcohol use, he may have alcoholic
pseudo-Cushing’s syndrome. This disorder can mimic endogenous Cushing’s
syndrome and can only be distinguished from it by having the patient
abstain from alcohol for an extended period of time. No evaluation for
Cushing’s syndrome should be done until after a period of abstinence.
The patient’s easy bruising can be explained by excess circulating cortisol.
Small vessel vasculitis would produce “palpable purpura” not found in this
patient. von Willebrand’s disease could produce bruising but not his other
symptoms. Platelet dysfunction would produce petechiae, not bruising.
Hemochromatosis would be expected to produce liver function
abnormalities, heart failure, diabetes, decreased libido, and a bronze
discoloration of the skin but not the hypertension, round face, and abnormal
fat deposition of Cushing’s syndrome.
A healthy 52-year-old woman is evaluated for her routine
annual physical examination. On physical examination, she is
162 cm (64 in) tall and weighs 60 kg (130 lb); her pulse rate is
80/min, and her blood pressure is 160/100 mm Hg. On two
subsequent days, she has her blood pressure measured and the
results are in the same range.
Laboratory studies show the following:
Serum sodium 140 meq/LSerum potassium 3.3 meq/LSerum
creatinine 0.8 mg/dLPlasma glucose 78 mg/dL
Which of the following is the most likely diagnosis?
( A ) Primary hyperaldosteronism
( B ) Renovascular hypertension
( C ) Pheochromocytoma
( D ) Bartter’s syndrome
( E ) Cushing’s syndrome
Correct Answer = A
This patient presents with the typical features of primary
hyperaldosteronism (autonomous overproduction of
aldosterone). Most patients with this disorder are
asymptomatic, and it should be considered in all patients with
hypertension and hypokalemia.
A paired plasma aldosterone concentration to plasma renin
activity ratio of greater than 20 is suggestive of this disorder,
and referral to a specialist is advisable because some patients
can be cured with unilateral adrenalectomy. Although Cushing’s
syndrome may cause hypertension and hypokalemia, there are
no suggestive clinical features of this disorder on the patient’s
history and physical examination. Renovascular hypertension
and pheochromocytoma are not associated with hypokalemia.
Bartter’s syndrome is associated with hypokalemia but not
hypertension.
Lifestyle modifications
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Should be prescribed to all patients including those in the “prehypertension” range – ie. 120-140 systolic 80-90 diastolic, and really
all of your patients of a certain age with or without other
cardiovascular risk factors
Weight reduction
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Diet
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Reduce to <2.4g sodium per day can reduce BP by 2-8mmHg
Exercise
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Reduce saturated fat
Increase fruit and vegetable content
Can reduce BP by 8-14 mmHg
Sodium restriction
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aim for BMI 18.5-24.9
Loss of 10 Kg can reduce BP by up to 20mmHg
Aerobic physical activity eg walking for 30 mins per day – can reduce BP by
4-9mmHg
Limiting alcohol
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<1 drink per day in women, <2 drinks per day in men can reduce BP by 24mmHg
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Thiazides
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Useful in cardiac pts, diabetics and certain pts with renal disease
Sometimes less helpful in african americans
Usually recommended that you check Chem 7 prior to starting and a couple of
weeks into treatment as pts with renal artery stenosis can get rising creatinines
and dangerously high K
Calcium channel blockers
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Useful in pts with heart failure and post MI, generally not used in diabetic
patients on sulfonylureas due to concerns that the β blocker masks the
symptoms of hypoglycemia. Also contraindicated in pts with bronchospasm
Watch for postural hypotension, can cause impotence, pts may complain of
feeling “tired”
ACE inhibitors
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First line in most patients, but risk of gout, impaired glucose tolerance,
impotence and many pts don’t like them due to urinary effect
β blockers
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Drug choices
Generally not first line now, but usually well tolerated.
Remember that many patients need two medications to adequately control BP.
Pt should be scheduled for follow up visit six weeks after starting med or
changing dose and then dose titrated accordingly.
A 47-year-old man who has had type 1 diabetes
mellitus for 23 years is found to have hypertension
that has been unresponsive to dietary salt restriction.
His physical examination shows a blood pressure of
144/94 mm Hg and background retinopathy.
His creatinine, blood urea nitrogen, and potassium are
normal. A 24-h urine albumin excretion rate is 152
mg. A second urine sample is also positive for
albumin, which measures 85 mg/24 h.
Which one of the following medications should
be used to treat this patient’s blood pressure?
( A ) Thiazide diuretic
( B ) Central sympatholytic agent
( C ) Angiotensin-converting enzyme (ACE) inhibitor
( D ) Calcium-channel blocker
Correct Answer = C
Several medications are effective in treating hypertension in patients with
diabetes. Angiotensin-converting enzyme (ACE) inhibitors, however, have
been shown to have selective benefit in this regard: they not only lower
blood pressure, but also can retard the rate of progression of any underlying
nephropathy.
In this patient, the presence of microalbuminuria (albumin level greater than
40 mg/24 h) indicates the presence of early nephropathy. Because ACE
inhibitors can retard the progression of nephropathy even in normotensive
individuals, these agents should be given even if nonpharmacologic therapy
has been successful in lowering the blood pressure to normal levels.
However, such use can cause hyperkalemia, and because patients with
diabetes are prone to hyporeninemic hypoaldosteronism (type IV renal
tubular acidosis), it is important to check potassium levels during therapy.
Other agents lack this selective benefit and are used as second-line
treatment or if ACE inhibitors cannot be tolerated.
A 48-year-old woman was found to have primary hypertension
6 months ago. Despite a trial of lifestyle modifications, her
blood pressure remained elevated at about 158/96 mm Hg.
Therapy with amlodipine, 5 mg daily, was begun.
The patient returns for a follow-up visit 6 weeks after beginning
amlodipine. Several blood pressures readings in the office
average 152/92 mm Hg. She has also noted progressive ankle
edema since therapy was begun.
Which of the following is most appropriate at this time?
(
(
(
(
A ) No change in therapy
B ) Change to another antihypertensive agent
C ) Increase the amlodipine to 10 mg daily
D ) Recommend a low-salt diet and support hose
Correct Answer = B
This patient’s blood pressure control while on amlodipine is inadequate (blood
pressure has not been reduced to < 140/90 mm Hg), and she has developed pedal
edema attributable to the dihydropyridine calcium-channel blocker.
Her medication should be changed to another antihypertensive agent that is unlikely
to induce edema and will optimize blood pressure control.
Adequate control of blood pressure to < 140/90 mm Hg is achieved in only 45% of
patients treated with medication, which represents only 27% of all patients with
hypertension. This has been labeled the “great hypertension disconnect.” Almost all
physicians know the target blood pressure of < 140/90 mm Hg; however, we are not
very successful in achieving this target.
When target blood pressure is not attained there are three possible options: 1)
increase the dose of the initial agent, 2) add a second agent, or 3) change to
another drug or class of agent.
This patient requires a change to another antihypertensive agent to achieve a target
blood pressure and reduce side effects. Increasing this patient’s dihydropyridine
calcium-channel blocker is not indicated because this will likely increase her edema.
A recent randomized, double-blind, clinical trail demonstrated that thiazide diuretics
were superior to calcium channel blockers or angiotensin-converting enzyme
inhibitors in lowering systolic blood pressure. The diuretic was superior to calcium
channel blockers in preventing heart failure, and superior to angiotensin-converting
enzyme inhibitors in reducing combined coronary vascular disease outcomes, stroke,
and heart failure. Since diuretics are less expensive and more effective in preventing
1 or more major forms of coronary vascular disease, they should be preferred for
first-step anti-hypertensive therapy in most patients. Finally, salt restriction and
support hose are unlikely to resolve the medication-induced edema or improve the
blood pressure.
A 56-year-old man is seen for routine follow-up of
hypertension. He has no complaints. He denies any recent
change in health status or drug use. His has been prescribed a
four-drug regimen of diltiazem sustained-release (SR),
captopril, atenolol, and hydrochlorothiazide. He is taking all his
medications. At his last clinic visit 2 months ago, his pulse rate
was 68/min, and his blood pressure was 138/86 mm Hg. He
has no other medical problems.
On physical examination, his pulse rate is 86/min and his blood
pressure is 194/116 mm Hg. The rest of his physical
examination is unremarkable. A stat complete blood count,
electrolytes, blood urea nitrogen, creatinine, glucose levels, and
urinalysis are all normal.
Which of the following is the most reasonable,
immediate office-treatment option?
( A ) Captopril and hydrochlorothiazide, orally
( B ) Nifedipine, sublingually
( C ) Lorazepam, orally
( D ) Nitroprusside, intravenously
( E ) No change in medications, follow-up in 2 weeks
Correct Answer = A
The most common cause of accelerated or urgent hypertension is
noncompliance with prescribed therapy, despite frequent patient claims to
the contrary.
Reasonable blood pressure control at the previous visit suggests that the
regimen was effective. The fact that the pulse rate is now 86/min casts
some doubt on whether the atenolol has been taken recently. Immediate
administration of some or all of the patient’s medications will help reestablish that they are effective for this patient.
It is not necessary to lower the blood pressure to normal at this juncture.
The use of sublingual nifedipine to lower blood pressure has been
condemned by medical experts and the U.S. Food and Drug Administration.
The precipitous and uncontrolled decrease in blood pressure frequently
produced by sublingual nifedipine presents a risk of myocardial infarction,
stroke, or death. Because the patient has no evidence of acute end-organ
damage (papilledema, abnormal mental status or neurologic findings),
admission to the intensive care unit for treatment of hypertensive crisis is
not warranted. Anxiety is not evident, nor is it likely to produce this
magnitude of blood pressure elevation; thus, treatment with lorazepam is
not indicated. Asking the patient to resume treatment with all medications
(option E) is reasonable, but the follow-up period of 2 weeks is
unreasonably long. It would be preferable to verify that the patient’s
regimen is effective before sending him home.
Lipids
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Check fasting lipoprotein analysis after 9-12
hour fast
Should be done at first visit to you and then
Ideal values:
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LDL < 130
Total cholesterol <200
TG <200
HDL >40
When instituting and following Tx, your first aim
should be to control LDL. If once LDL is
controlled the pt still has high TG then consider
adding nicotinic acid or fibrate
ATP III GUIDELINES
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STEP 1: Determine lipid level after 9-12 hr.
fast
STEP 2: Identify CHD risk equivalents
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Clinical CHD
AAA
Symptomatic carotid artery disease
PAD
ATP III Guidelines
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STEP 3: Determine major risk factors
other than LDL
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Cigarette smoking
BP>140/90 or on anti-HTN Rx
Low HDL (<40)
Family Hx CHD (<65 females, < 55 males)
Age (men >45, women >55)
ATP III Guidelines
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STEP 4: If 2+ risk factors (other than LDL)
present without CHD/CHD risk equivalent,
assess 10-year CHD risk (Framingham)
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>20%: CHD risk equivalent
10-20%
<10%
Framingham Risk Scores
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Method for assessing how aggressive you
should be at lowering lipids.
Based on risk factors identified in the
Framingham study.
Includes age, smoking, BP and both total
and HDL cholesterol and assigns a score
for each result, then dependent on total
score you can calculate 10 year risk of
having cardiovascular event
ATP III Guidelines
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STEP 5: Determine risk category
ATP III Guidelines
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STEP 6: Institute Lifestyle Changes
Very High Risk of CAD
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Goal LDL should be <70:
-pt with established CAD
PLUS
-multiple risk factors (DM)
OR
-severe, poorly-controlled risk factors
OR
-multiple risk factors of the metabolic
syndrome
OR
-acute coronary syndrome
ATP III Guidelines
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STEP 7: Consider adding drug therapy
(simultaneously with lifestyle changes if
CHD/CHD equivalents)
The Drugs
Drug
Action
Side effects
HMG CoA reductase
inhibitors (STATINS)
Reduce LDL by 18-50%
Increase HDL by 5-15%
Reduce TG by 7-30%
Myopathy – warn your pts
to come in for CK check if
muscle pain
LFT abnormalities –
contraindicated in liver
disease
Bile Acid
Sequestrants (eg.
Cholestyramine)
Reduce LDL by 15-30%
Increase HDL by 3-5%
No effect on TG
GI upset
Affect absorption of other
drugs
Don’t use in high TG – other
drugs are better
Nicotinic Acid
Reduce LDL by 5-25%
Increase HDL by 15-35%
Reduce TG by 25-50%
Main SE is flushing – tell
them to take their aspirin
right before
Can ppt gout, DM, hepatic
toxicity
Fibric acids
Reduce LDL by 5-20%
Increase HDL by 10-20%
Reduce TG by 20-50%
High risk of myopathy when
combined with statins.
CI in renal and liver disease
Can ppt gallstones
ATP III Guidelines
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STEP 8: Identify metabolic syndrome, and
treat, if present 3 months after TLC
ATP III Guidelines
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STEP 9: Treat elevated triglycerides
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Therapeutic lifestyle modifications
Primary aim is to reach LDL goal
If still high after LDL goal is reached, set HDL
goal 30 mg/dL higher than LDL goal 
intensify statin or add nicotinic acid or fibrate
Preguntas
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1. 65 yo male with BPH, actively smoking,
210 lbs, comes for his first physical since
1978. BP: 148/92. Lipid panel: T chol:
208, LDL: 135, HDL 38, TG: 130
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What are his goals?
How do you get him there?
What can we do to help you stop
smoking?
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Ask every pt at every visit whether they are smoking and
how much and document in the chart
Find out whether they want to quit
Ask what you can do to help them quit
Only 5-8% of smokers can quit on their own
Advice from a doctor can improve the smoking cessation
rate by 2.5%
Quitting smoking can decrease risk of death from CAD
by 50% in the first year of cessation
Cancer risk decreases to risk of 30 to 50% compared to
people who continue to smoke after 10 years
Hazards of Smoking Cessation
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Withdrawal symptoms
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Depression
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Peak in 1-3 days after cessation
Cravings can last months
Mild, but may still require counseling, treatment, or
return to smoking
Weight gain
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Often 1-2 kg in first 2 weeks with additional 2-3 kg
over the next 4-5 months
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Integrate dietary interventions with smoking cessation
Exacerbations of Ulcerative Colitis
Drug
Adjuncts in smoking cessation
Issues
Dosing
Nicotine gum
Main problem is compliance –
they have to be using pretty
much continuously.
<25 cigarettes per day
use 2mg, >25 cigarettes
per day use 4mg
Use 1-2 tabs per hour for
4-6 weeks
Nicotine patch
Main SE is insomnia – tell pt to
remove the patch at night
21mg/d for 6weeks then
14mg/d for 2 weeks then
7mg/d for 2 weeks
Wellbutrin
Can be used in addtion to the
patch or gum and treats the
concomitant depression
associated with stopping
smoking
Contraindicated in seizures,
alcohol abuse, anorexia,
150mg bid – start 1-2
weeks prior to the quit
date and continue for 712 weeks.
Varenicline (Chantix)
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Novel partial agonist of nicotinic
acetylcholine receptors
Better than bupropron and placebo at 12
wks and 52 wks
Side effects: nausea, abnormal dreams
Questions?